aphidicolin and monodansylcadaverine

Stress-responsive genes play critical roles in many biological functions that includes apoptosis, survival, differentiation and regeneration. We have identified a novel stress-responsive gene called BRE which interacts with TNF-receptor-1 and blocks the apoptotic effect of TNF-alpha. BRE enhances tumor growth in vivo and is up-regulated in hepatocellular and esophageal carcinomas. BRE also regulates the ubiquitination of the DNA repair complex BRCC, and the synthesis of steroid hormones. Here, we examined BRE-mRNA in cells after treatments with UV and ionizing radiation (IR). UV and IR treatment alone suppressed BRE-mRNA levels by more than 90% at 24 h, while hydroxyurea, fluorodeoxyuridine, aphidicolin, known inhibitors of S-phase DNA synthesis, had no significant effect. BRE protein expression was unaltered in cells treated with TNF-alpha, Interleukin-1 and Dexamethasone, while a threefold increase was observed following chorionic gonadotropin exposure. Although BRE plays a regulatory role in many different pathways, yet its expression is apparently under very stringent control.

Topics: Aphidicolin; Biological Factors; Cadaverine; Cell Line; Chorionic Gonadotropin; Dexamethasone; Dimethyl Sulfoxide; DNA Ligase ATP; DNA Ligases; Fluorodeoxyuridylate; Gene Expression Regulation; Humans; Hydroxyurea; Interleukin-1; Nerve Tissue Proteins; Nuclear Proteins; Promyelocytic Leukemia Protein; Radiation, Ionizing; RNA, Messenger; Signal Transduction; Stress, Physiological; Transcription Factors; Tumor Necrosis Factor-alpha; Tumor Suppressor Proteins; Ultraviolet Rays